Expression Of Jenes Bim And P-JNK Signaling Transduction Pathway In Rat Brain Follwing Cerebral Ischemia

PrefaceBerebral ischemia is a common pathologic processs, which threatens the wealth and life of human being, Its mechanism is still unclear. Previous studies show that JNK is intensively related with cerebral ischemia reperfusion lesion. Recently, the apoptosis protein Bim is founded in neuron, it is located in 7p15. 2 and encode the protein containing 129 amino acid. There is a few report about the relation between JNK and Bim. We study the JNK pathway and its relationship with Bim in cerebral ischemia reperfusion lesion.MethodsTo construct the model of rat cerebral ischemia reperfusion lesion, collect the tissues of dentate gyrus of rats and make coronal sections, observe the number of apoptosis cells in hippocampus under light microscope. To examine the apoptotic pyramidal neuron by TUNEL test and the expression of Bim and p -JNK in different groups by immuno - blotting test.ResultsThe apoptosis rate and the necrosis rate in ischemia reperfusion groups are significantly higher than that of control(P <0. 05) , apoptotic neuron was found in hippocampus neurons, and the number increase with the elongation of the time of reperfusion, peaked in 2h and then decreased gradually. But there is no difference between IRⅣ and IRⅤ ( P > 0.05 ).The expression of p - JNK in ischemia reperfusion groups was different tothat of control ( P < 0. 05 ) , and increased with the elongation of the time of reperfusion, peaked in 12h, then decreased gradually.The expression of Bim in ischemia reperfusion groups was different to that of control(P <0. 05) , and increased with the elongation of the time of reperfusion, peaked in 2h, then decreased gradually. The expression was significantly decreased in 24h after the reperfusion( P <0.05).The JNK pathway was over activated during the cerebral ischemia and the reperfusion lesion, the expression of p -JNK was increased.The expression of p — JNK was positively related to that of Bim, it is to say that, the activation of JNK pathway resulted in the increase of Bim expression.The peak of Bim expression(IRlI) appeared at the same time of the peak of neuron apoptosis (IRII ) , but the peak of p - JNK expression was late than that of Bim.ConclusionsThe apoptosis rate and the necrosis rate in ischemia reperfusion groups are significantly higher than that of control.The JNK pathway was over activated during the cerebral ischemia and the reperfusion lesion, the expression of p - JNK was increased.The expression of p - JNK was positively related to that of Bim.The activation of JNK pathway resulted in the increase of Bim expression, which induce the increase of the apoptosis of neuron, showing that during the apoptosis of neuron depended on JNK, Bim is an important partcipant.